Diabetes is a disease that still has no known cure. There are many surprising things that researchers have been learning about this condition. One of the recent findings indicate that diabetes may in fact start in the intestines.
Researchers from the Washington University School of Medicine in St. Louis may have found a surprising origin for diabetes. Their studies suggest that the body’s problem handling and controlling blood sugar levels may begin in the intestines. The said study involved mice models and might change some long-held theories about the origins of diabetes. The study findings are published in the February issue of Cell Host and Microbe.
Previous theories about diabetes based its origins on the organs such as the pancreas, where insulin is produced, and the liver, where sugar is stored. Scientists have focused on these organs in order to try and learn more about the underlying causes of diabetes. But the new research suggests that it may also be coming from the other organs.
In the said research, scientists studied mice with the inability to make fatty acid synthase or FAS in the intestine. This enzyme is an essential compound in the production of lipids. FAS is also regulated by insulin. It is also known that people with diabetes also show certain defects on FAS. The researchers found out that mice without the said enzyme in the intestines went on to develop chronic inflammation in the gut, which is known as a powerful predictor of diabetes.
Insulin resistance and inflammation are known to be associated with each other. Substances known to cause inflammation can also cause insulin resistance and affect the production of insulin in the body. And in the same way, insulin resistance is also known to promote inflammation.
“Diabetes may indeed start in your gut,” according to Clay F. Semenkovich, MD, the Herbert S. Gasser Professor of Medicine, professor of cell biology and physiology and director of the Division of Endocrinology, Metabolism and Lipid Research. “When people become resistant to insulin, as happens when they gain weight, FAS doesn’t work properly, which causes inflammation that, in turn, can lead to diabetes,” he further added.
Dr. Semenkovich, along with first author Xiaochao Wei, PhD, worked together with specialists in gastroenterology and genome sciences in order to find out what happens in mice when they do not have the ability to make FAS in their intestines. What the researchers found out is that the mice developed diarrhea and other gastrointestinal symptoms at the same time when started losing weight. When the researchers looked more closely inside the intestines, they observed some considerable inflammation that also made the mice sick.
The initial assumption was that it was the imbalance of the microbes in the gut that caused the mice to lose weight and get sick. But the researchers found out that the mice without FAS also lost the protective lining of mucus in the intestines that separates the healthy cells from the harmful microbes. The thinning mucus lining caused the microbes to get direct exposure to the healthy cells that led to the mice getting sick in the process.
“Fatty acid synthase is required to keep that mucosal layer intact,” Wei, a research instructor in medicine and also the study’s first author, states. “Without it, bad bacteria invade cells in the colon and the small intestine, creating inflammation, and that, in turn, contributes to insulin resistance and diabetes.”
Semenkovich and Wei both agree that further studies are needed but also say that FAS and the intestinal component may also be a potential target for diabetes therapy in the future.
Source: Washington University in St. Louis (2012, February 15). Diabetes may start in the intestines, research suggests. ScienceDaily. Retrieved March 1, 2012, from http://www.sciencedaily.com/releases/2012/02/120215123352.htm
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